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Neurology > Neuro12 Pharmacology > Flashcards

Neuro12 Pharmacology Flashcards

1
Q

Glaucoma drugs: alpha-agonists: Epinephrine

A

MOA: decreases aqueous humor synthesis clue to
vasoconstriction

Side effects: Mydriasis, stinging; do not use in closed-angle glaucoma

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2
Q

Glaucoma drugs: alpha-agonists: Brimonidine

A

MOA: decreases aqueous humor synthesis

Side effects: No pupillary or vision changes

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3
Q

Glaucoma drugs: Beta-blockers: Timolol, betaxolol, carteolol

A

MOA: decreases aqueous humor secretion

Side effects: No pupillary or vision changes

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4
Q

Glaucoma drugs: Diuretics: Acetazolamide

A

MOA: decreases aqueous humor secretion due to decreased HC03-

Side effects: No pupillary or vision changes
(via inhibition of carbonic anhydrase)

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5
Q

Glaucoma drugs: Cholinomimetics: Direct (pilocarpine, carbachol), indirect (physostigmine,
echothiophate)

A

MOA: increases outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening meshwork into canal of Schlemm

Side effect: Miosis, cyclospasm

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6
Q

Glaucoma drugs: Prostaglandin: Latanoprost (PGF2aplha)

A

MOA: increases outflow of aqueous humor

Side effect: Darkens color of iris (browning)

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7
Q

Opioid analgesics: Morphine, fentanyl, codeine, heroin, methadone, meperidine, clextromethorphan, diphenoxylate

A

MOA: Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission-open K+ channels, close Ca2+ channels leads to decreased synaptic transmission. Inhibit release of ACh, NE, 5 -HT, glutamate, substance P.

Clinical use: Pain, cough suppression (dextromethorphan), diarrhea (loperamicle and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone).

Toxicity: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist) .

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8
Q

Butorphanol

A

MOA: Partial agonist at opioid m u receptors, agonist at kappa receptors.

Clinical use: Pain; causes less respiratory depression than full agonists.

Toxicity: Causes withdrawal if on full opioid agonist.

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9
Q

Tramadol

A

MOA: Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters-“tram it all” in).

Clinical use: Chronic pain

Toxicity: Similar to opioids. Decreases seizure threshold.

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10
Q

Phenytoin

A

Use:
Partial Seizures: Simple, Complex
Generalized: 1st line for Tonic-clonic, 1st line prophylaxis for Status

MOA: Increases Na+ channel inactivation

Fosphenytoin for parenteral use

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11
Q

Carbamazepine

A

Use:
Partial: 1st line for Simple, 1st line for Complex
Generalized: 1st line for Tonic-clonic

MOA: Increases Na+ channel inactivation

1st line for Trigeminal neuralgia

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12
Q

Lamotrigine

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Blocks voltage-gated Na+ channels

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13
Q

Gabapentin

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Designed as GABA analog, but primarily inhibits HVA Ca2+ channels

Also used for peripheral neuropathy, bipolar disorder

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14
Q

Topiramate

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Blocks Na+ channels, increases GABA action

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15
Q

Phenobarbital

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: increases GABA-A action

1st line in children with partial or tonic-clonic seizures

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16
Q

Valproic acid

A

Use:
Partial Seizures: Simple, Complex
Generalized: 1st line in Tonic-clonic, Absence

MOA: increases Na+ channel inactivation, increases GABA concentration

Also used for myoclonic seizures

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17
Q

Ethosuximide

A

Use: 1st line for Absence Seizures

MOA: Blocks thalamic T-type Ca2+ channels

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18
Q

Benzodiazepines (diazepam or lorazepam)

A

Use: 1st line for acute Status seizures

MOA: increases GABA-A action

Also used for seizures of eclampsia (1st line is MgSO4

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19
Q

Tiagabine

A

Use:
Partial Seizures: Simple, Complex

MOA: Inhibits GABA reuptake

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20
Q

Vigabatrin

A

Use:
Partial Seizures: Simple, Complex

MOA: Irreversibly inhibits GABA transaminase which leads to an increase GABA

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21
Q

Levetiracetam

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Unknown; may modulate GABA and glutamate
release

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22
Q

Benzodiazepines toxicities

A

Sedation, tolerance, dependence.

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23
Q

Carbamazepine toxicities

A

Diplopia, ataxia, blood dyscrasias
(agranulocytosis, aplastic anemia), liver
toxicity, teratogenesis, induction of cytochrome
P-450, SIADH, Stevens-Johnson syndrome.

Stevens-Johnson syndrome-prodrome of
malaise and fever followed by rapid onset of
erythematous/purpuric macules (oral, ocular,
genital) . Skin lesions progress to epidermal
necrosis and sloughing.

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24
Q

Ethosuximide toxicities

A

GI distress, fatigue, headache, urticaria,
Stevens-Johnson syndrome.

EFGH - Ethosuximide, Fatigue, GI, Headache.

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25
Q

Phenobarbital toxicities

A

Sedation, tolerance, dependence, induction of cytochrome P-450.

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26
Q

Phenytoin toxicities

A

Nystagmus, diplopia, ataxia, sedation, gingival
hyperplasia, h irsutism, megaloblastic anemia,
teratogenesis (fetal hydantoin syndrome), SLElike
syndrome, induction of cytochrome P-450.

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27
Q

Valproic acid toxicities

A

GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain.
Contraindicated in pregnancy.

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28
Q

Lamotrigine toxicities

A

Stevens-Johnson syndrome

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29
Q

Gabapentin toxicities

A

Sedation, ataxia.

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30
Q

Topiramate toxicities

A

Sedation, mental dulling, kidney stones, weight loss.

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31
Q

Phenytoin

A

Use: Tonic-clonic seizures. Also a class IB antiarrhythmic.

MOA: Use-dependent blockade of Na+ channels; decreases refractory period; inhibition of glutamate release from excitatory presynaptic neuron.

Toxicity: Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic
use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic
anemia ( -1- folate absorption) . Teratogenic (fetal hydantoin syndrome).

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32
Q

Barbiturates

A

Phenobarbital, pentobarbital, thiopental, secobarbital.

Use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

MOA: Facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuron firing.

BarbiDU RATe (increases DURATion) .

Contraindicated in porphyria.

Toxicity: Dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450). Treat overdose with symptom management (assist respiration, increases BP) .

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33
Q

Benzodiazepines

A

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.

Use: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

MOA: Facilitate GABA-A action by increasing frequency of Cl channel
opening. decreases REM sleep. Most have long half-lives and active metabolites.

FREnzodiazepines (i FREquency) .
Short acting = TOM Thumb = Triazolam, Oxazepam, Midazolam. Highest addictive potential.

Benzos, barbs, and EtOH all bind GABA(A) -R, which is a ligand-gated chloride channel.

Toxicity: Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor) .

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34
Q

Nonbenzodiazepine hypnotics

A

Zolpidem (Ambien), zaleplon, eszopiclone.

Use: Insomnia.

MOA: Act via the BZ1 receptor subtype and are reversed by flumazenil.

Toxicity: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Lower dependence risk than benzodiazepines.

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35
Q

Anesthetics-general principles

A

CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
Drugs with decreased solubility in blood = rapid induction and recovery times.

Drugs with increased solubility in lipids = increased potency = 1/MAC

MAC = minimal alveolar concentration at which 50% of the population is anesthetized. Varies with age.
Examples: N20 has low blood and lipid solubility, and thus fast induction and low potency.
Halothane, in contrast, has increased lipid and blood solubility, and thus high potency and slow induction.

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36
Q

Effect of Anesthetics on Lungs

A

increases rate + depth of ventilation = increases gas tension

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37
Q

Effect of Anesthetics on Blood

A

increases blood solubility = increases blood/gas partition coefficient = increases solubility = increases gas required to saturate blood = slower onset of action

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38
Q

Effect of Anesthetics on Tissue (e.g., brain)

A

AV concentration gradient increases = increases solubility = increases gas required to saturate tissue = slower onset of
action

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39
Q

Inhaled anesthetics

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.

MOA: Unknown

Effects: Myocardial depression, respiratory depression, nausea/emesis, increases cerebral blood flow (decreases cerebral metabolic demand) .

Toxicity: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant
hyperthermia (rare), expansion of trapped gas (nitrous oxide) .

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40
Q

Intravenous anesthetics

A

Barbiturates, Benzodiazepines, Arylcyclohexylamines (Ketamine), Opiates, Propofol

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41
Q

Barbiturates: Thiopental

A

Thiopental: high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures.
Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. decreases cerebral blood flow.

B. B. King on O PIATES PROPOses FOOLishly.

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42
Q

Benzodiazepines: Midazolam

A

Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decreases BP
(treat overdose with flumazenil), and amnesia.

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43
Q

Arylcyclohexylamines

Ketamine

A

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. increases cerebral blood flow.

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44
Q

Opiates

A

Morphine, fentanyl used with other CNS depressants during general anesthesia.

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45
Q

Propofol

A

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A

Not recommended for home use by pop stars.

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46
Q

Local anesthetics

A

Esters-procaine, cocaine, tetracaine; amides-lldocalne, meplvacalne, buplvacalne (amldes have 2 l’s in name)

MOA: Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

Principle:

l. In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane
effectively. More anesthetic is needed in these cases.
2. Order of nerve blockade-small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers. Order of loss-pain (lose first) > temperature > touch > pressure (lose last) .
3. Except for cocaine, given with vasoconstrictors (usually epinephrine) to enhance local action decreases bleeding, increases anesthesia by decreases systemic concentration.

Use: Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

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47
Q

Neuromuscular blocking drugs

A

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

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48
Q

Depolarizing Neuromuscular blocking drugs

A

Succinylcholine (complications include hypercalcemia and hyperkalemia) .
Reversal of blockade:
Phase I (prolonged depolarization) -no antidote. Block potentiated by cholinesterase inhibitors.
Phase II (repolarized but blocked) -antidote consists of cholinesterase inhibitors (e.g., neostigmine).

49
Q

Nondepolarizing Neuromuscular blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium. Competitive: compete with ACh for receptors.
Reversal of blockade-neostigmine, edrophonium, and other cholinesterase inhibitors.

50
Q

Dantrolene

A

Use: Used in the treatment of malignant hyperthermia, which is caused by inhalation anesthetics (except N20) and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs) .

MOA: Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

51
Q

Parkinson’s disease drugs

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

BALSA:
Bromocriptine
Amantadine
Levodopa (with carbidopa)
Selegiline (and COMT inhibitors)
Anti muscarinics
For essential or familial tremors, use a
52
Q

Bromocriptine

A

Bromocriptine (ergot), pramipexole, ropinirole
(non-ergot) ; non-ergots are preferred

Strategy: Agonize dopamine receptors

53
Q

Amantadine

A

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia

Strategy: increases dopamine

L-dopa/carbidopa (converted to dopamine in CNS)

54
Q

Selegiline

A

Selegiline (selective MAO type B inhibitor); entacapone, tolcapone (COMT inhibitorsprevent L-dopa degradation, thereby increasing dopamine availability)

Strategy: Prevent dopamine breakdown

55
Q

Benztropine

A

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)

Strategy: Curb excess cholinergic activity

Park your Mercedes-Benz

56
Q

L-dopa (levodopa)/ carbidopa

A

Use: Parkinsonism

MOA: increases level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.

Toxicity: Arrhythmias from peripheral conversion to dopamine. Long-term use can lead to dyskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to i the bioavailability of L-dopa in the brain and to limit peripheral side effects.

57
Q

Selegiline

A

Use: Adjunctive agent to L-dopa in treatment of Parkinson’s disease.

MOA: Selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5 -HT, thereby increasing the availability of dopamine

Toxicity: May enhance adverse effects of L-dopa.

58
Q

Alzheimer’s drugs

A

Memantine, Donepezil, galantamine, rivastigmine

59
Q

Memantine

A

Use: Alzheimers

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

Toxicity: Dizziness, confusion, hallucinations.

60
Q

Donepezil, galantamine, rivastigmine

A

Use: Alzheimers

MOA: Acetylcholinesterase inhibitors.

Toxicity: Nausea, dizziness, insomnia.

61
Q

Huntington’s drugs

A

Disease: increases dopamine, decreases GABA + ACh.
Reserpine + tetrabenazine -amine depleting.
Haloperidol: dopamine receptor antagonist.

62
Q

Sumatriptan

A

Use: Acute migraine, cluster headache attacks.

MOA: 5-HTIB/ID agonist. Causes vasoconstriction,
inhibition of trigeminal activation and vasoactive peptide release. Half-life < 2 hours.

A SUMo wrestler TRIPs ANd falls on your head.

Toxicity: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal’s angina), mild tingling.

63
Q

Opioid analgesics: Morphine, fentanyl, codeine, heroin, methadone, meperidine, clextromethorphan, diphenoxylate

A

MOA: Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission-open K+ channels, close Ca2+ channels leads to decreased synaptic transmission. Inhibit release of ACh, NE, 5 -HT, glutamate, substance P.

Clinical use: Pain, cough suppression (dextromethorphan), diarrhea (loperamicle and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone).

Toxicity: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist) .

64
Q

Butorphanol

A

MOA: Partial agonist at opioid m u receptors, agonist at kappa receptors.

Clinical use: Pain; causes less respiratory depression than full agonists.

Toxicity: Causes withdrawal if on full opioid agonist.

65
Q

Tramadol

A

MOA: Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters-“tram it all” in).

Clinical use: Chronic pain

Toxicity: Similar to opioids. Decreases seizure threshold.

66
Q

Phenytoin

A

Use:
Partial Seizures: Simple, Complex
Generalized: 1st line for Tonic-clonic, 1st line prophylaxis for Status

MOA: Increases Na+ channel inactivation

Fosphenytoin for parenteral use

67
Q

Carbamazepine

A

Use:
Partial: 1st line for Simple, 1st line for Complex
Generalized: 1st line for Tonic-clonic

MOA: Increases Na+ channel inactivation

1st line for Trigeminal neuralgia

68
Q

Lamotrigine

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Blocks voltage-gated Na+ channels

69
Q

Gabapentin

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Designed as GABA analog, but primarily inhibits HVA Ca2+ channels

Also used for peripheral neuropathy, bipolar disorder

70
Q

Topiramate

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Blocks Na+ channels, increases GABA action

71
Q

Phenobarbital

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: increases GABA-A action

1st line in children with partial or tonic-clonic seizures

72
Q

Valproic acid

A

Use:
Partial Seizures: Simple, Complex
Generalized: 1st line in Tonic-clonic, Absence

MOA: increases Na+ channel inactivation, increases GABA concentration

Also used for myoclonic seizures

73
Q

Ethosuximide

A

Use: 1st line for Absence Seizures

MOA: Blocks thalamic T-type Ca2+ channels

74
Q

Benzodiazepines (diazepam or lorazepam)

A

Use: 1st line for acute Status seizures

MOA: increases GABA-A action

Also used for seizures of eclampsia (1st line is MgSO4

75
Q

Tiagabine

A

Use:
Partial Seizures: Simple, Complex

MOA: Inhibits GABA reuptake

76
Q

Vigabatrin

A

Use:
Partial Seizures: Simple, Complex

MOA: Irreversibly inhibits GABA transaminase which leads to an increase GABA

77
Q

Levetiracetam

A

Use:
Partial Seizures: Simple, Complex
Generalized: Tonic-clonic

MOA: Unknown; may modulate GABA and glutamate
release

78
Q

Benzodiazepines toxicities

A

Sedation, tolerance, dependence.

79
Q

Carbamazepine toxicities

A

Diplopia, ataxia, blood dyscrasias
(agranulocytosis, aplastic anemia), liver
toxicity, teratogenesis, induction of cytochrome
P-450, SIADH, Stevens-Johnson syndrome.

Stevens-Johnson syndrome-prodrome of
malaise and fever followed by rapid onset of
erythematous/purpuric macules (oral, ocular,
genital) . Skin lesions progress to epidermal
necrosis and sloughing.

80
Q

Ethosuximide toxicities

A

GI distress, fatigue, headache, urticaria,
Stevens-Johnson syndrome.

EFGH - Ethosuximide, Fatigue, GI, Headache.

81
Q

Phenobarbital toxicities

A

Sedation, tolerance, dependence, induction of cytochrome P-450.

82
Q

Phenytoin toxicities

A

Nystagmus, diplopia, ataxia, sedation, gingival
hyperplasia, h irsutism, megaloblastic anemia,
teratogenesis (fetal hydantoin syndrome), SLElike
syndrome, induction of cytochrome P-450.

83
Q

Valproic acid toxicities

A

GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain.
Contraindicated in pregnancy.

84
Q

Lamotrigine toxicities

A

Stevens-Johnson syndrome

85
Q

Gabapentin toxicities

A

Sedation, ataxia.

86
Q

Topiramate toxicities

A

Sedation, mental dulling, kidney stones, weight loss.

87
Q

Phenytoin

A

Use: Tonic-clonic seizures. Also a class IB antiarrhythmic.

MOA: Use-dependent blockade of Na+ channels; decreases refractory period; inhibition of glutamate release from excitatory presynaptic neuron.

Toxicity: Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic
use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic
anemia ( -1- folate absorption) . Teratogenic (fetal hydantoin syndrome).

88
Q

Barbiturates

A

Phenobarbital, pentobarbital, thiopental, secobarbital.

Use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

MOA: Facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuron firing.

BarbiDU RATe (increases DURATion) .

Contraindicated in porphyria.

Toxicity: Dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450). Treat overdose with symptom management (assist respiration, increases BP) .

89
Q

Benzodiazepines

A

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.

Use: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

MOA: Facilitate GABA-A action by increasing frequency of Cl channel
opening. decreases REM sleep. Most have long half-lives and active metabolites.

FREnzodiazepines (i FREquency) .
Short acting = TOM Thumb = Triazolam, Oxazepam, Midazolam. Highest addictive potential.

Benzos, barbs, and EtOH all bind GABA(A) -R, which is a ligand-gated chloride channel.

Toxicity: Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor) .

90
Q

Nonbenzodiazepine hypnotics

A

Zolpidem (Ambien), zaleplon, eszopiclone.

Use: Insomnia.

MOA: Act via the BZ1 receptor subtype and are reversed by flumazenil.

Toxicity: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Lower dependence risk than benzodiazepines.

91
Q

Anesthetics-general principles

A

CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
Drugs with decreased solubility in blood = rapid induction and recovery times.

Drugs with increased solubility in lipids = increased potency = 1/MAC

MAC = minimal alveolar concentration at which 50% of the population is anesthetized. Varies with age.
Examples: N20 has low blood and lipid solubility, and thus fast induction and low potency.
Halothane, in contrast, has increased lipid and blood solubility, and thus high potency and slow induction.

92
Q

Effect of Anesthetics on Lungs

A

increases rate + depth of ventilation = increases gas tension

93
Q

Effect of Anesthetics on Blood

A

increases blood solubility = increases blood/gas partition coefficient = increases solubility = increases gas required to saturate blood = slower onset of action

94
Q

Effect of Anesthetics on Tissue (e.g., brain)

A

AV concentration gradient increases = increases solubility = increases gas required to saturate tissue = slower onset of
action

95
Q

Inhaled anesthetics

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.

MOA: Unknown

Effects: Myocardial depression, respiratory depression, nausea/emesis, increases cerebral blood flow (decreases cerebral metabolic demand) .

Toxicity: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant
hyperthermia (rare), expansion of trapped gas (nitrous oxide) .

96
Q

Intravenous anesthetics

A

Barbiturates, Benzodiazepines, Arylcyclohexylamines (Ketamine), Opiates, Propofol

97
Q

Barbiturates: Thiopental

A

Thiopental: high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures.
Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. decreases cerebral blood flow.

B. B. King on O PIATES PROPOses FOOLishly.

98
Q

Benzodiazepines: Midazolam

A

Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decreases BP
(treat overdose with flumazenil), and amnesia.

99
Q

Arylcyclohexylamines

Ketamine

A

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. increases cerebral blood flow.

100
Q

Opiates

A

Morphine, fentanyl used with other CNS depressants during general anesthesia.

101
Q

Propofol

A

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A

Not recommended for home use by pop stars.

102
Q

Local anesthetics

A

Esters-procaine, cocaine, tetracaine; amides-lldocalne, meplvacalne, buplvacalne (amldes have 2 l’s in name)

MOA: Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

Principle:

l. In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane
effectively. More anesthetic is needed in these cases.
2. Order of nerve blockade-small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers. Order of loss-pain (lose first) > temperature > touch > pressure (lose last) .
3. Except for cocaine, given with vasoconstrictors (usually epinephrine) to enhance local action decreases bleeding, increases anesthesia by decreases systemic concentration.

Use: Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

103
Q

Neuromuscular blocking drugs

A

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

104
Q

Depolarizing Neuromuscular blocking drugs

A

Succinylcholine (complications include hypercalcemia and hyperkalemia) .
Reversal of blockade:
Phase I (prolonged depolarization) -no antidote. Block potentiated by cholinesterase inhibitors.
Phase II (repolarized but blocked) -antidote consists of cholinesterase inhibitors (e.g., neostigmine).

105
Q

Nondepolarizing Neuromuscular blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium. Competitive: compete with ACh for receptors.
Reversal of blockade-neostigmine, edrophonium, and other cholinesterase inhibitors.

106
Q

Dantrolene

A

Use: Used in the treatment of malignant hyperthermia, which is caused by inhalation anesthetics (except N20) and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs) .

MOA: Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

107
Q

Parkinson’s disease drugs

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

BALSA:
Bromocriptine
Amantadine
Levodopa (with carbidopa)
Selegiline (and COMT inhibitors)
Anti muscarinics
For essential or familial tremors, use a
108
Q

Bromocriptine

A

Bromocriptine (ergot), pramipexole, ropinirole
(non-ergot) ; non-ergots are preferred

Strategy: Agonize dopamine receptors

109
Q

Amantadine

A

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia

Strategy: increases dopamine

L-dopa/carbidopa (converted to dopamine in CNS)

110
Q

Selegiline

A

Selegiline (selective MAO type B inhibitor); entacapone, tolcapone (COMT inhibitorsprevent L-dopa degradation, thereby increasing dopamine availability)

Strategy: Prevent dopamine breakdown

111
Q

Benztropine

A

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)

Strategy: Curb excess cholinergic activity

Park your Mercedes-Benz

112
Q

L-dopa (levodopa)/ carbidopa

A

Use: Parkinsonism

MOA: increases level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.

Toxicity: Arrhythmias from peripheral conversion to dopamine. Long-term use can lead to dyskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to i the bioavailability of L-dopa in the brain and to limit peripheral side effects.

113
Q

Selegiline

A

Use: Adjunctive agent to L-dopa in treatment of Parkinson’s disease.

MOA: Selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5 -HT, thereby increasing the availability of dopamine

Toxicity: May enhance adverse effects of L-dopa.

114
Q

Alzheimer’s drugs

A

Memantine, Donepezil, galantamine, rivastigmine

115
Q

Memantine

A

Use: Alzheimers

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

Toxicity: Dizziness, confusion, hallucinations.

116
Q

Donepezil, galantamine, rivastigmine

A

Use: Alzheimers

MOA: Acetylcholinesterase inhibitors.

Toxicity: Nausea, dizziness, insomnia.

117
Q

Huntington’s drugs

A

Disease: increases dopamine, decreases GABA + ACh.
Reserpine + tetrabenazine -amine depleting.
Haloperidol: dopamine receptor antagonist.

118
Q

Sumatriptan

A

Use: Acute migraine, cluster headache attacks.

MOA: 5-HTIB/ID agonist. Causes vasoconstriction,
inhibition of trigeminal activation and vasoactive peptide release. Half-life < 2 hours.

A SUMo wrestler TRIPs ANd falls on your head.

Toxicity: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal’s angina), mild tingling.

Neurology (12 decks)

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